Song-Shei Lin

China Medical University Hospital, 臺中市, Taiwan, Taiwan

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Publications (24)39.91 Total impact

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    ABSTRACT: The Non-homologous end-joining repair gene XRCC6/Ku70 plays an important role in the repair of DNA double-strand breaks (DSBs), and has been found to be involved in the carcinogenesis of many types of cancers including oral, prostate, breast and bladder cancer. However, the contribution of XRCC6 to childhood leukemia has yet to be studied. In the present study, we investigated the association of XRCC6 genotypes with the risk of childhood leukemia. Two hundred and sixty-six patients with childhood leukemia and an equal number of age-matched healthy controls recruited in Central Taiwan, were genotyped investigating these polymorphisms' association with childhood leukemia. As for XRCC6 promoter T-991C, patients carrying the TC genotype had a significantly increased risk of childhood leukemia compared with the TT wild-type genotype [odds ratio (OR)=2.30, 95% confidence interval (CI)=1.38-3.84, p=0.0047]. Meanwhile, the genotypes of XRCC6 promoter C-57G, A-31G and intron3 were not statistically associated with childhood leukemia risk. Our findings suggest that the XRCC6 genotype could serve as a predictor of childhood leukemia risk and XRCC6 could serve as a target for personalized medicine and therapy.
    Anticancer research 12/2013; 33(12):5395-5399. · 1.71 Impact Factor
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    ABSTRACT: Aim: Upper urothelial tract cancer is unusually of high incidence in Taiwan and it is valuable to study the specificity of this disease in Taiwan and compare the corresponding findings with those of Western countries. In the literature, it has been reported that single nucleotide variation of caveolin-1 gene (CAV1) plays an important role in risk of several types of cancer, such as hepatoma, leukemia, nasopharyngeal carcinoma, oral, breast, bladder and prostate cancer, but we are not aware of any reports on upper urothelial tract cancer. The aim of this study was to evaluate the association of six polymorphic genotypes of CAV1 with upper urothelial tract cancer within a Taiwanese population. A total of 218 patients with upper urothelial tract cancer and 580 healthy controls in central Taiwan were genotyped by polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP) for six CAV1 polymorphic genotypes, C521A (rs1997623), G14713A (rs3807987), G21985A (rs12672038), T28608A (rs3757733), T29107A (rs7804372), and G32124A (rs3807992), and their association with upper urothelial tract cancer susceptibility was examined. The distribution of genotypes of CAV1 rs3807987 and rs7804372 were significantly different between cancer patient and control groups (p=0.0188 and 0.0090, respectively), while those for CAV1 rs1997623, rs12672038, rs3757733 and rs3807992 were not significant (p>0.05). The haplotype analysis of the two polymorphic genotypes showed that compared with the GG/AT, and GG/AA haplotypes of CAV1 rs3807987/rs7804372, those carrying GG/TT, AG/TT and AA/TT variants have a significantly increased risk of upper urothelial tract cancer (odds ratio=1.61, 1.50 and 2.67, 95% confidence interval=1.05-2.47, 1.18-1.90, and 1.37-5.18, respectively). On the contrary, other haplotype variants conferred non-significant elevated risk. Our results suggest that individual and combined CAV1 rs3807987/rs7804372 genotypes are involved in predisposition to upper urothelial tract cancer in the Taiwanese population.
    Anticancer research 11/2013; 33(11):4907-4912. · 1.71 Impact Factor
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    ABSTRACT: Amentoflavone, isolated from an ethyl acetate extract of the whole plant of Selaginella tamariscina, a traditional herb, may exhibit antitumor activity. The aim of this study was to investigate the anticancer mechanism(s) of amentoflavone, such as mitochondria-mediated apoptotic cell death, in typical breast cancer MCF-7 cells. Cells treated with amentoflavone exhibited a series of cellular alterations related to apoptosis, including DNA and nuclear fragmentation, and de-regulation of intracellular reactive oxygen species (ROS) and calcium. In addition, markers of mitochondrial-mediated apoptosis, including the reduction of mitochondrial inner-membrane potential, the release of cytochrome c from mitochondria, and activation of caspase 3, were observed. In conclusion, our results present, to our knowledge, the first evidence that amentoflavone induces apoptosis of MCF-7 breast cancer cells, and that this is closely related to mitochondrial dysfunction. Amentoflavone may be a potential therapeutic agent for breast cancer treatment.
    In vivo (Athens, Greece) 11/2012; 26(6):963-970. · 1.15 Impact Factor
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    ABSTRACT: The antitumor effects of curcumin, a natural biologically active compound extracted from rhizomes of Curcuma longa, have been studied in many cancer cell types including human hepatocellular carcinoma (HCC). Here, we investigated the effects of Ca(2+) on curcumin-induced apoptosis in human HCC J5 cells. The abrogation of mitochondrial membrane potential (ΔΨ(m)), the increase of reactive oxygen species (ROS) production, and calcium release were demonstrated with flow cytometry as early as 15 minutes after curcumin treatment. In addition, an increase level of cytochrome c in the cytoplasm which led to DNA fragmentation was observed. To verify the role of Ca(2+) in curcumin-induced apoptosis, 1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA), an intracellular calcium chelator, was applied. Cell viability was increased, but ΔΨ(m), ROS production, activation of caspase 3, and cell death were decreased in J5 cells pretreated with BAPTA for 2 h followed by the treatment of 25 μM curcumin. These results suggest that the curcumin-induced apoptosis in human HCC J5 cells is via mitochondria-dependent pathway and is closely related to the level of intracellular accumulation of calcium.
    Evidence-based Complementary and Alternative Medicine 01/2012; 2012:512907. · 1.72 Impact Factor
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    ABSTRACT: Diallyl sulfide (DAS), one of the main active constituents of garlic, causes growth inhibition of cancer cells in vitro and promotes immune responses in vivo in experimental settings. However, its effects on the induction of cell cycle and apoptosis in human cervical cancer cells are still unclear. The aims of this study were to explore the anti-cancer effects of DAS in HeLa human cervical cancer cells and to investigate the underlying mechanisms in vitro. Cytotoxicity and apoptosis in HeLa human cervical cancer cells were examined by the morphological changes, viability assay, 4',6-Diamidino-2-phenylindole dihydrochloride (DAPI) staining, comet assay, Western blotting and confocal microscopy examination. The results showed that DAS treatment for 24-72 h resulted in a marked decrease in cell viability time- and dose-dependently. Flow cytometric analysis showed that a 48-h treatment of 75 µM DAS induced G0/G1 cell cycle arrest and sub-G1 phase (apoptosis) in HeLa cells. Typical apoptotic nucleus alterations were observed by fluorescence microscopy in HeLa cells after exposure to DAS using DAPI staining. Cells treated with different concentrations of DAS also showed changes typical of apoptosis such as morphological changes, DNA damage and fragmentation, dysfunction of mitochondria, cytochrome c release and increased expression of pro-caspase-3 and -9. DAS also promoted the release of AIF and Endo G from mitochondria in HeLa cells. In conclusion, DAS induced G0/G1 cell cycle arrest and apoptosis in HeLa cells through caspase- and mitochondria and p53 pathways providing further understanding of the molecular mechanisms of DAS action in cervical cancer. This study, therefore, revealed that DAS significantly inhibits the growth and induces apoptosis of human cervical cancer HeLa cells in vitro.
    International Journal of Oncology 03/2011; 38(6):1605-13. · 2.66 Impact Factor
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    ABSTRACT: Ultraviolet (UV) radiation is a natural insult to various organisms. Earthworms, although possessing similar biomolecules to those in mammalian skin, do not suffer from skin cancer nor any other types of cancer as humans do. However, little is known about the molecular mechanism of the earthworm's tolerance to UV. In this study, we evaluated the genotoxicity of UV and the capacity of earthworm cell to repair UV-induced damage. The T4 UV endonuclease UV-incorporated comet assay was used to examine the excision and rejoining steps of UV-induced pyrimidine dimer. Earthworm testis cells were treated with a combination of 5 mM hydroxyurea plus 50 μM cytosine-β-D-arabinofuranoside for 6 h to block DNA rejoining capacity and to investigate excision dynamics. Compared with H(2)O(2)-induced oxidative repair capacity, the excision step of repair of UV-induced lesions in earthworm testis cells was significantly lower. After 6-h treatment of 5 mM hydroxyurea plus 50 μM cytosine-β-D-arabinofuranoside, the medium was totally replaced with fresh medium and cells were allowed to rejoin the accumulated DNA strand breaks. We found that the capacity for rejoining UV-induced breaks was also significantly lower than that for the H(2)O(2)-induced breaks. Our results strongly suggest that earthworms seem to be efficient at repairing H(2)O(2)-induced oxidative DNA adducts, but not so capable of removing UV-induced pyrimidine dimers from their genome.
    In vivo (Athens, Greece) 01/2011; 25(6):977-81. · 1.15 Impact Factor
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    ABSTRACT: The anti-tumor properties of arsenic trioxide have attracted extensive attention after successfully inducing apoptosis of acute promyelocytic leukemia cells. However, the therapeutic spectrum should not only be restricted to acute promyelocytic leukemia, but should also extend into other types of tumor cells. In this study, we aimed at investigating its potential application to clinical therapeutics in oral cancer. In this preclinical animal test, primarily cultured cells from the tumor sites and normal sites of a two-drug (200 μg/ml 4-nitroquinoline 1-oxide (4NQO) plus 500 μg/ml arecoline)-induced oral cancer C57BL/6J Narl mice model were examined for their viabilities after treatments of arsenic trioxide with/without other drugs. In this model, the mice were treated with 4NQO plus arecoline (NA) in their drinking water for eight weeks (8-w), and the drugs were withdrawn for another 10 or 20 weeks (18-w and 28-w, respectively). The results showed that 2 μM of arsenic trioxide 24-h treatment suppressed the viabilities of cells primarily cultured from the tumor sites of 8-w, 18-w and 28-w NA-treated mice to 72.9%, 71.5% and 65.6%. However, it also suppressed the viabilities of cells from the sham-treated mice of 8-w, 18-w and 28-w to 76.8%, 73.4% and 75.7%, respectively. Therefore, 0.5 μM of arsenic trioxide treatment for 24 h, which suppressed the viabilities of cells primarily cultured from the tumor sites of 28-w NA-treated and sham-treated mice to 15.6% and 9.1%, was examined for its synergistic effects on the two primarily cultured cell lines with other drugs. The results showed that 10-20 μM dithiothreitol enhanced the cytotoxic effects of arsenic trioxide to 43.3~62.1%, better than those of 4 J/m(2) UVC, 20 μM H(2)O(2) or 100 μM buthionine sulfoximine (21.3%, 13.2%, and 14.2%, respectively). At the same time, 10-20 μM dithiothreitol plus 0.5 μM arsenic trioxide treatments caused only 12.3% and 15.2% of cell death in the control group. The cytotoxicity of dithiothreitol and arsenic trioxide combination on primarily cultured cells from this oral cancer model should be confirmed in human oral cancer cell lines before its application in clinical therapy, and the detailed mechanism is worth further investigation.
    Anticancer research 09/2010; 30(9):3655-60. · 1.71 Impact Factor
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    ABSTRACT: The DNA repair gene X-ray repair complementing defective repair in Chinese hamster cells 4 (XRCC4) is thought to play a major role in the caretaking of the whole genome via double-strand break repair. However, the association of polymorphic variants of XRCC4 with colorectal cancer susceptibility has never been reported. In this hospital-based case-control study, the association of XRCC4 polymorphisms C-1622T (rs7727691), G-1394T (rs6869366), G-652T (rs2075685), C-571T (rs2075686), intron 3 DIP (rs28360071), S247A (rs3734091) and intron 7 DIP (rs28360317) with colorectal cancer risk in a Taiwanese population was investigated. The genotypes of XRCC4 of 370 patients with colorectal cancer and 370 age- and gender-matched healthy controls were determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis. We found significant differences in the genetic and allelic frequencies of the XRCC4 G-1394T between the colorectal cancer and control groups (p=0.0003 and 8.32 x 10(-5), respectively). The distributions of other genetic polymorphisms between cases and the control group were not significantly different. We conclude that the G allele of XRCC4 G-1394T may contribute to colorectal carcinogenesis and may be useful for early detection of colorectal cancer.
    Anticancer research 07/2010; 30(7):2727-30. · 1.71 Impact Factor
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    ABSTRACT: It is well known that matrix metalloproteinases (MMPs) act an important role in the invasion, metastasis and angiogenesis of cancer cells. Agents suppressed the MMPs could inhibited the cancer cells migration and invasion. Numerous evidences had shown that curcumin (the active constituent of the dietary spice turmeric) has potential for the prevention and therapy of cancer. Curcumin can inhibit the formation of tumors in animal models of carcinogenesis and act on a variety of molecular targets involved in cancer development. There is however, no available information to address the effects of curcumin on migration and invasion of human lung cancer cells. The anti-tumor invasion and migration effects of lung cancer cells induced by curcumin were examined. Here, we report that curcumin suppressed the migration and invasion of human non-small cell lung cancer cells (A549) in vitro. Our findings suggest that curcumin has anti-metastatic potential by decreasing invasiveness of cancer cells. Moreover, this action was involved in the MEKK3, p-ERK signaling pathways resulting in inhibition of MMP-2 and -9 in human lung cancer A549 cells. Overall, the above data shows that the anticancer effect of curcumin is also exist for the inhibition of migration and invasion in lung cancer cells.
    Cancer letters 06/2009; 285(2):127-33. · 5.02 Impact Factor
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    ABSTRACT: In this study, we investigated the effects of DADS on human colon cancer cell line COLO 205 on cell cycle arrest and apoptosis in vitro. After 24 h treatment of COLO 205 cells with DADS, the dose- and time-dependent decreases of viable cells were observed and the IC50 was 22.47 μM. The decreased percentages of viable cells are associated with the production of ROS. Treatment of COLO 205 cells with DADS resulted in G2/M phase arrest and apoptosis occurrence through the mitochondrial-pathway (Bcl-2, Bcl-xL down-regulation and Bak, Bax up-regulation). DADS increased cyclin B, cdc25c-ser-216-9 and Wee1 but did not affect CDK1 protein and gene expression within 24 h of treatment. DADS-induced apoptosis was examined and confirmed by DAPI staining and DNA fragmentation assay. DADS promoted caspase-3, -8 and -9 activity and induced apoptosis were accompanied by increasing the levels of Fas, phospho-Ask1 and -JNK, p53 and decreasing the mitochondrial membrane potential which then led to release the cytochrome c, cleavage of pro-caspase-9 and -3. The COLO 205 cells were pre-treated with JNK inhibitor before leading to decrease the percentage of apoptosis which was induced by DADS. Inhibition of caspase-3 activation blocked DADS-induced apoptosis on COLO 205 cells.
    Food and chemical toxicology: an international journal published for the British Industrial Biological Research Association 01/2009; · 2.99 Impact Factor
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    ABSTRACT: Curcumin, a major component of the Curcuma species, is known to have antioxidant, anti-inflammatory properties and induce apoptosis of cancer cells, however, the precise molecular mechanisms of apoptosis in vitro are unclear. In this study, we showed that curcumin, a plant product containing the phenolic phytochemical, caused DNA damage and endoplasmic reticulum (ER) stress and mitochondrial-dependent-induced apoptosis through the activation of caspase-3 at a treatment concentration of 30 microM in human lung cancer A-549 cells. In contrast, treatment with 5-10 microM of curcumin did not induce significant apoptosis, but rather induced G2/M-phase arrest in A-549 cells. Flow cytometric analysis indicated that curcumin directly increased intracellular oxidative stress based on the cell permeable dye, 2',7'-dichlorodihydrofluorescein diacetate (DCFH-DA) acting as an indicator of reactive oxygen species (ROS) generation. GADD153 and GRP78 were increased by curcumin which was indicative of ER stress. Curcumin increased Ca(2+) levels and the mitochondrial membrane potential (DeltaPsi(m)), was decreased in A-549 cells. Overall, our results demonstrated that curcumin treatment causes cell death by activating pathways inducing G2/M-phase arrest and apoptosis.
    Cancer letters 09/2008; 272(1):77-90. · 5.02 Impact Factor
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    ABSTRACT: The effects of oral luteolin on the N-acetylation and metabolism of 2-aminofluorene (AF) in vivo were investigated in bladder, blood, colon, kidney, liver, feces, urine, cerebrum, cerebellum and pineal gland from male Sprague-Dawley rats. Major metabolites such as AAF, 1-OH-AAF, 3-OH-AAF, 8-OH-AAF and 9-OH-AAF were found in bladder tissues; AAF, 1-OH-AAF, 5-OH-AAF and 8-OH-AAF were found in blood samples; AAF, 1-OH-AAF, 3-OH-AAF, 5-OH-AAF, 8-OH-AAF and 9-OH-AAF were found in colon tissues; AAF, 1-OH-AAF, 3-OH-AAF and 9-OH-AAF were found in kidney tissues; AAF, 1-OH-AAF, 3-OH-AAF and 8-OH-AAF were found in liver tissues, AAF, 1-OH-AAF, 3-OH-AAF, 5-OH-AAF, 7-OH-AAF, 8-OH-AA and 9-OH-AAF were found in feces and urine samples; AAF, 1-OH-AAF, 3-OH-AAF and 8-OH-AAF were found in cerebrum tissues; AAF, 1-OH-AAF, 3-OH-AAF and 7-OH-AAF were found in cerebellum tissues; but only AF and AAF were found in pineal gland in rats treated with AF (50 mg/kg) for 24 h. Pretreatment of rats with luteolin (30 mg/kg) 24 h prior to the administration of AF (50 mg/kg) and luteolin given with AF concomitantly led to a decrease in the amounts of 3-OH-AAF and 9-OH-AAF and an increase in the amounts of 1-OH-AAF and 8-OH-AAF in bladder tissues. In blood samples, there were significant decreases of AAF, 1-OH-AAF and 8-OH-AAF after rats were treated with luteolin for 24 h prior to AF but luteolin with AF at the same time caused an increase in 1-OH-AAF. In colon tissues, there were significant decreases of AF, 1-OH-AAF, 3-OH-AAF, 5-OH-AAF and 9-OH-AAF after rats were treated with luteolin for 24 h then AF but the amounts of AF, 1-OH-AAF, 5-OH-AAF and 9-OH-AAF decreased and AAF and 8-OH-AAF increased in rats treated with luteolin and AF at the same time. In kidney tissues, there were significant decreases of AF, AAF and 3-OH-AAF after rats were treated with both compounds at the same time, but luteolin for 24 h then AF treatment led to significant decreases of 3-OH-AAF. In liver samples, after rats were treated with luteolin and AF at the same time, the amounts of AAF and 1-OH-AAF significantly decreased but 8-OH-AAF increased. However, rats treated with luteolin for 24 h then with AF led to significant decreases of AAF, 1-OH-AAF and 3-OH-AAF. In feces samples, there were significant increases of AAF, 3-OH-AAF, 7-OH-AAF, 8-OH-AAF and 9-OH-AAF after rats were treated with both compounds at the same time but luteolin for 24 h then AF treatment led to a significant increase of AF, 1-OH-AAF and 8-OH-AAF and a decrease AAF and 3-OH-AAF. In urine samples, there were significant increases of AF, AAF, 1-OH-AAF, 3-OH-AAF, 5-OH-AAF and 9-OH-AAF but a decrease of 8-OH-AAF after rats were treated with both compounds at the same time. However, the luteolin for 24 h then AF treatment led to significant increases of AF, AAF and 1-OH-AAF but decreases of 3-OH-AAF and 5-OH-AAF. In cerebrum samples, there were significant increases ofAF but decreases of 1-OH-AAF and 8-OH-AAF after rats were treated with both compounds at the same time; luteolin for 24 h then AF treatment of rats led to significant increase of 1-OH-AAF and decreases AF, AAF and 8-OH-AAF. In cerebellum samples, there were significant increases of AAF and decreases of 1-OH-AAF and 3-OH-AAF after rats were treated with both compounds at the same time, there is a significant increase of AAF but decrease of 1-OH-AAF, 3-OH-AAF and 7-OH-AAF after the luteolin treated for 24 h then AF were treated to the rats. In pineal gland samples, there were significant increases ofAAF after rats were treated with both compounds at the same time. However, luteolin treated for 24 h then AF were treated to the rats which increase AAF but decrease AF.
    In vivo (Athens, Greece) 01/2008; 22(6):729-34. · 1.15 Impact Factor
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    ABSTRACT: Curcumin (diferuloylmethane), a phenolic compound from the plant Curcuma longa (Linn.) has been shown to exhibit antitumor activity and apoptosis in many human cancer cell lines including that of lung and liver cancer. In this study, curcumin was evaluated in BALB/c mice for its ability to inhibit pulmonary and liver adenoma formation and growth after they were orally treated with N-bis(2-hydroxypropyl)nitrosamine (DHPN). Animals were treated with DHPN in water for approximately 14 days before multiple doses of curcumin were given intraperitoneally. It was found that 200 microM curcumin reduced lung and liver tumor multiplicity by 37% (p<0.05) and 30% (p<0.05) respectively. The results indicated that curcumin significantly inhibited pulmonary and liver adenoma formation and growth in BALB/c mice. The precise mechanism by which curcumin inhibits lung and liver tumorigenesis remains to be elucidated. Thus, curcumin appears to be a promising new chemotherapeutic and preventive agent for lung and liver cancer induced by DHPN.
    In vivo (Athens, Greece) 01/2008; 22(6):781-5. · 1.15 Impact Factor
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    ABSTRACT: Baicalein was investigated for tumor cell-specific cytotoxicity, apoptosis-inducing activity and signal pathway against the MDA-MB-231 human breast cancer cell line. After the MDA-MB-231 cells had been treated with baicalein, trypan blue exclusion, propidium iodide (PI) assay and 4',6-diamidino-2-phenylindole (DAPI) were used to stain the dead cells and detect apoptosis, respectively. The effects of baicalein on the levels of reactive oxygen species (ROS), Ca2+ and mitochondrial membrane potential (deltapsim) on MDA-MB-231 cells were examined by flow cytometric assays. The ROS caused endoplasmic reticulum (ER) stress, confirmed by the increase of GADD153 and GRP78 in the examined cells. GADD153 and GRP78 increases were also confirmed by confocal laser microscopy examination and indicated that both proteins translocated to the nucleus. The effects of baicalein on the expression of apoptotic-regulated genes, such as Bcl-2 family and caspase, were detected by Western blotting. To further investigate the apoptotic pathway and the role of Ca2+ induced by baicalein, a caspase-3 inhibitor and Ca2+ chelator were used to block caspase-3 activity and Ca2+ in MDA-MB-231 cells. Baicalein induced apoptosis in a time-dependent effect through the inhibition of Bcl-2 expression, increased the levels of Bax, reduced the level of deltapsim, and promoted the cytochrome c release and caspase-3 activation. MDA-MB-231 cells were pretreated with BAPTA which reduced the levels of Ca2+, deltapsim and apoptosis. In conclusion, baicalein induced apoptosis via Ca2+ production, mitochondria-dependent and caspase-3 activation in MDA-MB-231 cells.
    Anticancer research 01/2008; 28(3A):1701-11. · 1.71 Impact Factor
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    ABSTRACT: Curcumin (1, 7-bis(4-hydroxy-3-methoxyphenyl)-1,6-heptadiene-3,5- dione), a natural polyphenol product of the plant Curcuma longa, exhibited potent inhibitory activities against proliferation, induced cell cycle arrest and exhibited the induction of apoptosis in several tumor cell lines. In our previous studies, we have shown that curcumin induced cell cycle arrest and apoptosis on human leukemia HL-60 and mouse leukemia WEHI-3 cells; there are no reports regarding whether or not it affects leukemia cells in vivo. In the present study, we investigated the effects of curcumin on WEHI-3 in BALB/c mice and the results indicated that curcumin reduces the percentage of Mac-3 marker, which is the precursor of macrophage. Curcumin induced significant effects on the population of B cells from murine leukemia in vivo. We also investigated the weights of spleen and liver from murine leukemia and the results showed that curcumin reduced the weight of the liver and spleen. From the pathological examinations, the effects of curcumin on the liver and spleen from mice after being injected with WEHI-3 cells were apparent. Both organs were enlarged. In conclusion, curcumin affect WEHI-3 cells in vivo.
    In vivo (Athens, Greece) 01/2008; 22(1):63-8. · 1.15 Impact Factor
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    ABSTRACT: Aloe-emodin has shown anti-neoplastic activity against some human cancer cell lines. This study aimed to explore the effects of aloe-emodin on the phagocytosis of macrophages, the activity of natural killer (NK) cells and the expression of cytokines in leukocytes from Sprague-Dawley rats. Leukocytes were collected, placed into culture plates and the functions of macrophages and NK cells and the percentage of viable cells were determined by flow cytometric analysis. Incubation of leukocytes with various concentrations of aloe-emodin caused a dose-dependent decrease of viable cells, a decrease of phagocytosis by macrophages, and a decrease of the activity of NK cells. Evaluation of cytokines in leukocytes by ELISA indicated that aloe-emodin increased the levels of interleukin (IL)-1beta and tumor necrosis factor (TNF)-alpha. The results were also confirmed by PCR assay for the mRNA expression of the examined cytokines.
    In vivo (Athens, Greece) 01/2006; 20(4):505-9. · 1.15 Impact Factor
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    ABSTRACT: The role of Ca2+ on the effects of capsaicin on human leukemia HL-60 cells in vitro and the molecular mechanisms of capsaicin-induced apoptosis were investigated. The flow cytometric analysis indicated that capsaicin decreased the percentage of viable HL-60 cells, via the induction of G0/G1-phase cell cycle arrest and apoptosis. Capsaicin-induced G0/G1-phase arrest involved the suppression of CDK2 and the cyclin E complex, which are check-point enzymes for cells moving from G0/G1- to S-phase. Capsaicin-induced apoptosis was associated with the elevation of intracellular reactive oxygen species and Ca2+ production, decreased the levels of mitochondrial membrane potential, promoted cytochrome c release and increased the activation of caspase-3. An intracellular Ca2+ chelator (BAPTA) significantly inhibited capsaicin-induced apoptosis. Capsaicin-induced apoptosis was time-and dose-dependent. These results suggest that the capsaicin-induced apoptosis of HL-60 cells may result from the activation of caspase-3 and the intracellular Ca2+ release pathway.
    Anticancer research 01/2006; 26(3A):1965-71. · 1.71 Impact Factor
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    ABSTRACT: The case of a patient with surgically proven internal herniation of a loop of ileum through the sigmoid mesocolon is described. This 66-year-old man presented clinically with acute lower abdominal pain and an elevated white blood cell count. A computed tomography (CT) scan showed a thickened bowel loop with "bird-beak" appearance in the pelvis, centered towards the medial side and lying aside the effaced sigmoid colon. We think this CT picture is highly suggestive of internal herniation of the ileum through the sigmoid mesocolon, which is a rare clinical entity.
    Journal of the Chinese Medical Association 05/2005; 68(4):195-7. · 0.75 Impact Factor
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    ABSTRACT: The effects of 5-methoxypsoralen (5-MOP) on the distribution and metabolism of chemical carcinogens such as 2-aminofluorene (AF) has not been previously reported. In this study, the influences of 5-MOP on the metabolism of AF in Sprague-Dawley (SD) rats were investigated. After receiving 5-MOP in 24 hours, AF was introduced into each animal by gastric intubation. After 12, 24, 48 and 72 hours the urine, feces, and cytosol of the liver, kidneys, stomach, colon, bladder and blood of rats were collected and assayed for AF and its metabolites by HPLC. Compared to the control regimen, 5-MOP caused an increase of the metabolites excreted in urine and feces. The largest dose of metabolites were excreted between 48-72 hours. The major metabolite excreted in the urine was 9-hydroxy-AAF (9-OH-AAF) and in the feces was 7-hydroxy-AAF (7-OH-AAF). There was no time-effect for the tissues, and the liver was the main target organ for the AF and its metabolites. The major residual metabolite of AF in the liver, kidneys, stomach, colon and bladder was 7-OH-AAF. In blood it was 9-OH-AAF. The bladder had the lowest metabolic residue in tissues, and blood played the role of transportation but was not the target organ. 5-MOP decreased the concentration of AF and its residual metabolites of liver, stomach, kidneys, bladder and blood at various times. 5-MOP increased the metabolism of AF in order to transform to ring-hydroxylated metabolites and increased excretion of the ring-hydroxylated metabolites, therefore decreasing AF and its residual metabolites in vivo. Although 5-MOP was shown to be an inhibitor of CYP 2A6 and CYP 2B1, somehow it causes an increase of activity in AF metabolism in vivo; it induces more CYPs involved in the metabolism of AF.
    In vivo (Athens, Greece) 01/2002; 16(3):201-13. · 1.15 Impact Factor
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    ABSTRACT: The present study was undertaken to determine the effect of acetylsalicylic acid acid on the in vitro N-acetyltransferase (NAT) enzyme activity and in vivo acetylation of 2-aminofluorene in laboratory rats. In the in vitro experiments, cytosols of blood, bladder, colon and liver cells, with or without acetylsalicylic acid co-treatment, showed different percentages of 2-aminofluorene acetylation. The data indicated that there was decreased NAT activity associated with increased acetylsalicylic acid in the cytosol reaction. In the in vitro experiments, values of apparent Km and Vmax decreased by 4% and 21%, respectively, for acetylation of AF in blood NAT, 28% and 31% for acetylation of AF in bladder NAT, 12% and 25% for acetylation of AF in colon NAT, and 50% and 35% for acetylation of AF in liver NAT. In the in vivo experiments, pretreatment with acetylsalicylic acid (50 mg/kg) 48 h prior to the administration of 2-aminofluorene (50 mg/kg) resulted in 24% and 28% decreases in the fecal and urinary recovery of N-acetyl-2-aminofluorene and a 26% decrease in the metabolic clearance of 2-aminofluorene to N-acetyl-2-aminofluorene. This is the first demonstration of acetylsalicylic acid (Aspirin) inhibition of arylamine N-acetyltransferase activity showing decreases in the N-acetylation of carcinogens in vivo.
    In vivo (Athens, Greece) 19(2):475-81. · 1.15 Impact Factor

Publication Stats

270 Citations
39.91 Total Impact Points

Institutions

  • 2008–2013
    • China Medical University Hospital
      • Department of Radiology
      臺中市, Taiwan, Taiwan
    • Buddhist Tzu Chi General Hospital
      T’ai-pei, Taipei, Taiwan
  • 2008–2012
    • Central Taiwan University of Science and Technology
      臺中市, Taiwan, Taiwan
  • 2006–2011
    • China Medical University (ROC)
      臺中市, Taiwan, Taiwan